L-Carnitine-L-Tartrate

The effects of L-carnitine L-tartrate supplementation on hormonal responses to resistance exercise and recovery.

The purpose of this investigation was to examine the influence of L-carnitine L-tartrate (LCLT) supplementation using a balanced, cross-over, placebo-controlled research design on the anabolic hormone response (i.e., testosterone [T], insulin-like growth factor-I, insulin-like growth factor-binding protein-3 [IGFBP-3], and immunofunctional and immunoreactive growth hormone [GHif and GHir]) to acute resistance exercise. Ten healthy, recreationally weight-trained men (mean +/- SD age 23.7 +/- 2.3 years, weight 78.7 +/- 8.5 kg, and height 179.2 +/- 4.6 cm) volunteered and were matched, and after 3 weeks of supplementation (2 g LCLT per day), fasting morning blood samples were obtained on six consecutive days (D1-D6). Subjects performed a squat protocol (5 sets of 15-20 repetitions) on D2. During the squat protocol, blood samples were obtained before exercise and 0, 15, 30, 120, and 180 minutes postexercise. After a 1-week washout period, subjects consumed the other supplement for a 3-week period, and the same experimental protocol was repeated using the exact same procedures. Expected exercise-induced increases in all of the hormones were observed for GHir, GHif, IGFBP-3, and T. Over the recovery period, LCLT reduced the amount of exercise-induced muscle tissue damage, which was assessed via magnetic resonance imaging scans of the thigh. LCLT supplementation significantly (p < 0.05) increased IGFBP-3 concentrations prior to and at 30, 120, and 180 minutes after acute exercise. No other direct effects of LCLT supplementation were observed on the absolute concentrations of the hormones examined, but with more undamaged tissue, a greater number of intact receptors would be available for hormonal interactions. These data support the use of LCLT as a recovery supplement for hypoxic exercise and lend further insights into the hormonal mechanisms that may help to mediate quicker recovery.

Androgenic responses to resistance exercise: effects of feeding and L-carnitine.

PURPOSE: The purpose of this investigation was to determine the effects of 3 wk of L-carnitine L-tartrate (LCLT) supplementation and post-resistance-exercise (RE) feeding on hormonal and androgen receptor (AR) responses.

METHODS: Ten resistance-trained men (mean+/-SD: age, 22+/-1 yr; mass, 86.3+/-15.3 kg; height, 181+/-11 cm) supplemented with LCLT (equivalent to 2 g of L-carnitine per day) or placebo (PL) for 21 d, provided muscle biopsies for AR determinations, then performed two RE protocols: one followed by water intake, and one followed by feeding (8 kcal.kg body mass, consisting of 56% carbohydrate, 16% protein, and 28% fat). RE protocols were randomized and included serial blood draws and a 1-h post-RE biopsy. After a 7-d washout period, subjects crossed over, and all experimental procedures were repeated.

Previous research has shown that L-carnitine L-tartrate (LCLT) supplementation beneficially affects markers of hypoxic stress following resistance exercise. However, the mechanism of this response is unclear. Therefore, the primary purpose of this study was to determine the effects of LCLT supplementation on muscle tissue oxygenation during and after multiple sets of squat exercise. Nine healthy, previously resistance-trained men (25.2 +/- 6.years, 91.2 +/- 10.2 kg, 180.2 +/- 6.3 cm) ingested 2 g.d of LCLT or an identical placebo for 23 days in a randomized, balanced, crossover, double-blind, placebo-controlled, repeated-measures study design. On day 21, forearm muscle oxygenation was measured during and after an upper arm occlusion protocol using near infrared spectroscopy (NIRS), which measures the balance of oxygen delivery in relation to oxygen consumption. On day 22, subjects performed 5 sets of 15 to 20 repetitions of squat exercise with corresponding measures of thigh muscle oxygenation, via NIRS, and serial blood draws. Compared to the placebo trial, muscle oxygenation was reduced in the LCLT trial during upper arm occlusion and following each set of resistance exercise. Despite reduced oxygenation, plasma malondealdehyde, a marker of membrane damage, was attenuated during the LCLT trial. There were no differences between trials in the vasoactive substance prostacyclin. In conclusion, because oxygen delivery was occluded during the forearm protocol, it is proposed that enhanced oxygen consumption mediated the reduced muscle oxygenation during the LCLT trial. Enhanced oxygen consumption would explain why hypoxic stress was attenuated with LCLT supplementation.

We examined the influence ofL-carnitine L-tartrate (LCLT) on markers of purine catabolism, free radical formation, and muscle tissue disruption after squat exercise. With the use of a balanced, crossover design (1 wk washout), 10 resistance-trained men consumed a placebo or LCLT supplement (2 g L-carnitine/day) for 3 wk before obtaining blood samples on six consecutive days (D1 to D6). Blood was also sampled before and after a squat protocol (5 sets, 15-20 repetitions) on D2. Muscle tissue disruption at the midthigh was assessed using magnetic resonance imaging (MRI) before exercise and on D3 and D6. Exercise-induced increases in plasma markers of purine catabolism (hypoxanthine, xanthine oxidase, and serum uric acid) and circulating cytosolic proteins (myoglobin, fatty acid-binding protein, and creatine kinase) were significantly (P &le; 0.05) attenuated by LCLT. Exercise-induced increases in plasma malondialdehyde returned to resting values sooner during LCLT compared with placebo. The amount of muscle disruption from MRI scans during LCLT was 41-45% of the placebo area. These data indicate that LCLT supplementation is effective in assisting recovery from high-repetition squat exercise.

Ten healthy, recreationally weight-trained men (mean +/- SD age 23.7 +/- 2.3 years, weight 78.7 +/- 8.5 kg, and height 179.2 +/- 4.6 cm) volunteered and were matched, and after 3 weeks of supplementation (2 g LCLT per day), fasting morning blood samples were obtained on six consecutive days (D1-D6). Subjects performed a squat protocol (5 sets of 15-20 repetitions) on D2. During the squat protocol, blood samples were obtained before exercise and 0, 15, 30, 120, and 180 minutes postexercise. After a 1-week washout period, subjects consumed the other supplement for a 3-week period, and the same experimental protocol was repeated using the exact same procedures. Expected exercise-induced increases in all of the hormones were observed for GHir, GHif, IGFBP-3, and T. Over the recovery period, LCLT reduced the amount of exercise-induced muscle tissue damage, which was assessed via magnetic resonance imaging scans of the thigh. LCLT supplementation significantly (p < 0.05) increased IGFBP-3 concentrations prior to and at 30, 120, and 180 minutes after acute exercise. No other direct effects of LCLT supplementation were observed on the absolute concentrations of the hormones examined, but with more undamaged tissue, a greater number of intact receptors would be available for hormonal interactions. These data support the use of LCLT as a recovery supplement for hypoxic exercise and lend further insights into the hormonal mechanisms that may help to mediate quicker recovery.

By David Barr
Through the haze of misinformation clouding the supplement industry, strength athletes are often left wondering if anything will actually help them. Recently, a little known supplement has emerged that can do just that. In this article, we'll take a look at this product and see how it can help with muscle growth, strength, and recovery.

Before we go any further, you need to know what we're talking about. The supplement in question is called carnitine-l-tartrate (CLT), and there's a good chance you'll be using it for a long time to come. It's different in both structure and mechanism of action from acetyl-l-carnitine, which is commonly sold as a fat loss supplement. So don't worry if you've tried "carnitine" as an over-hyped "fat burner" and were disappointed by the results.

What does it do? CLT is a unique supplement because it increases the androgen receptor content of tissues. This means that there are more docking sites for our most plentiful anabolic hormone to function. In short, more testosterone/androgens reaching their target = a greater anabolic effect.

This sounds pretty amazing, right? Almost too good to be true, huh? I appreciate such skepticism, and in fact, quite encourage it. However, fortunately we have a growing body of evidence for this one. Better still, this evidence comes from one of the most prestigious exercise labs on the planet, with each study showing the efficacy of this supplement (Kraemer, et al. 2003; Kraemer, et al. 2006; Volek, et al. 2002).

Enter the Anabolic Index Score

So just how effective is CLT? Using the Anabolic Index Score, which objectively measures the anabolic potential of foods and supplements, CLT ranks as one of the most potent products available. When combined with protein pulse feeding, especially after a workout, the impact on muscle growth is great. This combined effect is so powerful because post-training meals also increase androgen receptor content. So you're really maximizing the effect by combining the two (Kraemer, et al. 2006).

Quick Ttip: For those who are using HRT or other androgen related pharmaceuticals, CLT greatly increases the effectiveness of the cycle. In this situation, you would not only be gaining a pharmaceutically-induced elevation of androgen receptors but also a supplemental elevation.

Anabolism and recovery

We often get so wrapped up in our subculture that words adopt new meanings. Specifically in this case, I'm referring to anabolism (or "anabolic"), which is most commonly used in reference to muscle building, and ultimately, strength. Although this isn't completely inaccurate for our purposes, it ignores a critical component of anabolism--muscle recovery.

By increasing muscle anabolism, regardless of the means, we're definitively increasing the rate at which our muscle can recover from the training-induced stress we impose on it. Greater recovery means less down time and increased opportunity to incur the training stresses we seek (i.e. growth and strength). I'm sure you're probably well aware of this fact, but it never hurts to have an occasional reminder.

To sum things up, by increasing the androgen receptor content of our muscle, CLT will be able to assist with the following critical variables:

CLT is a legal supplement with potentially powerful effects on everything we want that is related to muscle. Better yet, it also has strong potential to improve neural strength and recovery--highly sought after processes that continue to elude us. Considering that we don't fully understand neural adaptability, there's much to be covered, which means that we'll be discussing this in the next article.

Neural Performance and Recovery with Carnitine-L-Tartrate
By David Barr
For www.EliteFTS.com

In the last article, we looked at the potential for a supplement called carnitine-l-tartrate (CLT) to improve muscle growth, strength, and recovery. In this article, we'll take a look at the theoretical basis for CLT to improve something even more elusive--neural performance and recovery.

CLT is the most bioavailable form of the common fat loss supplement carnitine. Although it's generally not marketed for performance and strength, recent data have emerged to suggest that it may play a positive role in these processes. Information on neural stress and recovery is limited, but a tenuous connection can be made between our applied physiology and supplementation.

Recall that CLT use results in both improved muscular performance and an increase in muscle testosterone receptors. The implications of the former are clear, but it is the latter effect that may be neurally ergogenic. That is because the more docking sites we have available for the anabolic hormone testosterone, the greater its ability to deliver its powerful message.

Getting neural

For the most part, exercise physiology has a decent understanding of muscle stress and recovery, which means that we have a few good ideas about how to improve or even optimize them. However, strength athletes are often more concerned about nervous system stresses, the details of which are far more obscure. After all, it's easy enough to perform some kind of exercise intervention and take a muscle biopsy to see what's going on. However, you can't just cut out someone's nerves for a study.

This lack of information is unfortunate considering that it is these nerve cells (a.k.a. neurons) that transmit all of the signals from our brain to our limbs (among other things). More specifically, it is our motor neurons that are in contact with our muscles, which deliver the message to contract. As we adapt in our training, our neurons are better able to transmit these signals, which is one of the more important mechanisms of becoming stronger, and we are better able to resist fatigue.

Androgenic adaptation

There are plenty of data to show the relation between testosterone and our neural development, protection, and adaptation. That is to say that androgens acting directly on our nerve cells are largely responsible for the changes that occur, and this can ultimately lead to performance. For example, during exogenous anabolic use, neurons grow in size. This size increase can lead to greater signal transmission to our working muscle as well as a resistance to neural fatigue (i.e. improved strength and strength endurance).

Interestingly, it is this specific "connection" or signaling area that ends up receiving much of the benefit from androgen use because this is where androgen receptor up-regulation occurs during androgen use. Again, more androgen receptors mean that more growth and recovery signals can be delivered to the cell.

Up-regulation: An ideal mechanism

If we consider the effect of increasing androgen uptake due to an increase in receptors, we can begin to see why this is such a powerful mechanism of action. In traditional hormonal manipulation schemes, it is our goal to increase the quantity of hormone in the blood. This transient effect usually has some kind of backlash in which the hormonal concentration is ultimately reduced, thus largely negating any positive outcome. However, by simply increasing the number of docking sites for the hormone, we're actually increasing the clearance of the hormone from the blood. This signals the brain that we're running low on that hormone after which more of it will be produced.

It's clear that this latter mechanism is not only far more elegant but also more effective for our purposes.

Putting it all together

The point of all of this is that an increase in androgen receptor content in our working nerve cells would ultimately result in positive adaptations for strength and performance. If you'll recall that CLT has the ability to elevate muscle androgen receptor content in response to training, the picture will become clearer.

If CLT can exert its protective effect on our working nerve cells, particularly at the level of the nerve-muscle connection, we'll reap the benefit of increased androgenic adaptation. In fact, if such an adaptation exists, this could be the first supplement available to improve neural functioning and recovery.

Because neural recovery is far more limiting to performance and training than muscle recovery, the implications are quite powerful.

Summary

Although direct evidence for the performance enhancing effect of CLT exists, there is a theoretical basis for this supplement to positively interact with our nerve cells. Such an interaction would entail an increase in androgen receptor content, which would lead to greater anabolic signal delivery. In turn, this would ultimately increase strength, performance, and recovery at the neural level.

Where do you get CLT? I've been asked this quite a bit lately so it's worth discussing here. CLT is a ubiquitous product. You simply have to read the actual label to ensure that the "l-carnitine" you're looking at is actually CLT.

How much do you use? I recommend starting with 1.5 grams per 200 lbs with a minimum of 1 gram for lighter athletes. Moving up from 200 lbs would involve non-linear scaling, depending on numerous factors. The optimization of such a protocol is currently in development, and I'll report on it shortly.

David Barr is widely recognized as an industry innovator, most recently for his work on developing the Anabolic Index nutrition system. As a strength coach and scientist, he brings a unique perspective to the areas of supplementation, diet, and training. He holds certifications with the NSCA as well as USA Track and Field.

I have been pondering about LCLT and its use in women. Over the years I've seen a lot of discussion about optimising natty test levels in women. LCLT should have the same effect of increasing androgen receptors in women as it does in men. So should LCLT be a staple for women whatever there physical goals? As it should aid women in their body composition efforts as well as boost athletic performance

I have been pondering about LCLT and its use in women. Over the years I've seen a lot of discussion about optimising natty test levels in women. LCLT should have the same effect of increasing androgen receptors in women as it does in men. So should LCLT be a staple for women whatever there physical goals? As it should aid women in their body composition efforts as well as boost athletic performance

It would theoretically have a lesser effect in women since receptors are far from limiting wrt testosterone

http://pescience.com/
http://selectprotein.com/
The above is my own opinion and does not reflect the opinion of PES

If im not mistaken there was an idea that the beneficial effects of LCLT was from the l-tartrate and had nothing to do with the carnitine

I hope this isn't a stupid question, but here it is anyways: even if that is the case would the bonding(assuming it's bonded) to carnitine possibly increase/decrease bioavailability? Meaning the carnitine could still be beneficial to the tartaric acid?

http://anabolicminds.com/forum/workout-logs/231713-rob112-3-means.html
"Train like a animal, think like a human"-RTS

The trimethylated amino acid l-carnitine plays a key role in the intramitochondrial transport of fatty acids for beta-oxidation and thus serves important functions in energy metabolism. Here, we have tested the hypothesis that l-carnitine, a frequently employed dietary supplement, may also stimulate hair growth by increasing energy supply to the massively proliferating and energy-consuming anagen hair matrix. Hair follicles (HFs) in the anagen VI stage of the hair cycle were cultured in the presence of 0.5-50 microm of l-carnitine-l-tartrate (CT) for 9 days. At day 9, HFs treated with 5 microm or 0.5 microm of CT showed a moderate, but significant stimulation of hair shaft elongation compared with vehicle-treated controls (P < 0.05). Also, CT prolonged the duration of anagen VI, down regulated apoptosis (as measured by TUNEL assay) and up regulated proliferation (as measured by Ki67 immunohistology) of hair matrix keratinocytes (P < 0.5). By immunohistology, intrafollicular immunoreactivity for TGFbeta2, a key catagen-promoting growth factor, in the dermal papilla and TGF-beta II receptor protein in the outer root sheath and dermal papilla was down regulated. As shown by caspase activity assay, caspase 3 and 7, which are known to initiate apoptosis, are down regulated at day 2 and day 4 after treatment of HFs with CT compared with vehicle-treated control indicating that CT has an immediate protective effect on HFs to undergo programmed cell death. Our findings suggest that l-carnitine stimulates human scalp hair growth by up regulation of proliferation and down regulation of apoptosis in follicular keratinocytes in vitro. They further encourage one to explore topical and nutraceutical administration of l-carnitine as a well-tolerated, relatively safe adjuvant treatment in the management of androgenetic alopecia and other forms of hair loss.

There's no reason to believe tartrate is ergogenic. It's addition to carnitine does improve carnitine uptake though. Increasing muscle carnitine via LCLT improves the rate of FA transport into the mitochondrial matrix, thus leading to more rapid ATP formation via b-oxidation and less purinergic degradation via hypoxanthine dumping, which occurs in response to high cellular AMP. This is how LCLT is:

1. Ergogenic
2. Cell-protective (xanthine oxidase creates ROS in detoxifying xanthine to uric acid...to make matters worse, it also acts on hypoxanthine -> xanthine, so you get a double whammy for each molecule of hypoxanthine)
3. Able to improve the VO2 max (hypoxia is also a trigger for hypoxanthine dumping)

So in the anecdotal realms, what sorts of effects are people noticing? This is one form I haven't tried yet.

It is honestly really hard to quantify as I don't notice really much physically. Being that it has all of those positive studies and is dirt cheap is how I justify cost. Maybe it is just me but I feel you would have to really be in tune with testing it on yourself for different periods of time to gauge without any type of lab testing on tissues, response to androgens in the body before and after use, etc.

Just my 2 cents.

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http://anabolicminds.com/forum/workout-logs/231713-rob112-3-means.html
"Train like a animal, think like a human"-RTS